Parkinson's disease!

[ofonorow]

. Therapies that focus on conversion of Glutamate to GABA, leading to normalcy of symptoms are mostly palliative and not curative.

Fascinating. It is wonderful to see how a brilliant MD functions when the reigns of Big Pharma are removedf! You are allowed to think, and your knowledge base is pretty wonderful.

7. Withdrawal occurs with ANY psychostimulants.

Before reading this, my wife and I stopped our coffee drinking cold turkey. NO HEADACHE.

I think this latest experience proves that the material in the Medical Medium books is accurate. The above quoted Medial Medium passage implied that caffeine blocked dopamine, and other brain hormones (causing the body to try an make more) and that this dopamine loss when coffee was withdrawn was the reason for the "brutal" withdrawal symptoms. The oracle did not recommend, but I got the idea to, take extra dopamine as we stopped the coffee; and it was miraculous. I was able to stop my wife and my coffee drinking - without any apparent withdrawal symptoms, i.e. NO headache!

For the record, this was the brand I happened to have and used:

https://www.amazon.com/gp/product/B009ANRU92/ref=ppx_yo_dt_b_asin_title_o00_s01?ie=UTF8&psc=1

The intriguing aspect is that first night, of not having any coffee or caffeine, my wife "woke up." Something like the movie "The Awakening". It was like she had come out of a daze, She was more conscious and started talking like I hadn't see her do in years. As if what the Medical Medium said about caffeine HARMING the brain, causing an adrenaline response to keep the brain from injury, is true. And IMO now, nobody with Parkinson's should be should be drinking coffee, especially with the knowledge how to mitigate the withdrawal/dependency. A little bit of dopamine supplement..

Now, our neurologist at the last visit diagnosed two conditions, Parkinson's and a kind of palsy, so the awakening was obviously in her awareness, but not yet in her motor skills. They do say it can take about 2 weeks (months?) for the brain to adjust to not having to deal with the caffeine poison daily.

I have gotten far enough in the Brain Saver book to learn that both Parkinson's and Alzheimer's are both caused by heavy metals. A fun fact is that most pharmaceuticals contain both heavy metals AND caffeine.

You eDOC have explained at least one of the components in the Medical Medium's Parkinson's Protocol:

GABA: 1 250-milligram capsule twice a day

Some other interesting components that may be related:

Kava Kava: 1 capsule (or dropper of a tincture) twice a day

L-glutamine: 2 capsules twice a day

Melatonin: work up to 20 milligrams at bedtime daily.

[ofonorow]

Quickly, your knowledge is human derived, mostly from experience. The Medical Medium knowledge is from "some where else." I suspect an advance science. And since you won't read it - we are at an impasse. They claim infallibility, so one time wrong, or anything in error, invalidates that premise. So far, after years, I haven't found ANYTHING wrong. And it all holds together, logically. If not an advanced science, only an AI could have written these books.

I didn't provide the entire Parkinson's supplement list, those that are interested can read the BRAIN SAVER book.

As far as the coffee, my wife had been getting up on average every two hours - and lately, some nights every hour.

Last night, she slept the entire night! Like a miracle. Knowing that caffeine blocks dopamine in the brain, it would be malpractice to not recommend that PD patient to get off caffeine.

[ofonorow]

TAURINE FOR PARKINSON'S DISEASE

After learning that "Chem Trails" are the deliberate release of toxic chemical wastes into the atmosphere, we started developing a new Detox product to be called DETOX-C (tm). The requirement for an ingredient Sulphur, i.e. sulfur containing aminos, such as cysteine and methionine) comes from reading TOXIC LEGACY by Senoff, a book about the problem with pesticides containing glyphosates.

This led to the normally non-essential amino Taurine (which the body makes from cysteine and methionine ) . This research led to the finding of Taurines benefit for Parkinson's:

Taurine and its analogs in neurological disorders: Focus on therapeutic potential and molecular mechanisms

https://www.sciencedirect.com/science/article/pii/S2213231719301971#:~:text=Taurine%20is%20a%20sulfur-containing%20amino%20acid%20and%20known,and%20demonstrates%20extensive%20physiological%20activities%20within%20the%20body.

4. Therapeutic potential of taurine against neurological disorders


4.2. Role in neurodegenerative diseases

.
.
.

In addition to the AD model, the neuroprotective action of taurine against Parkinson's disease (PD) has been studied in cellular and animal models. Taurine exerted an ameliorating action against rotenone-induced neurodegeneration [86,87]. It displayed a concentration-dependent reduction in rotenone-induced cell damage in SH-SY5Y cells. The combination of a subeffective dose of taurine and low and subeffective doses of N-acetyl cysteine afforded better cytoprotection against rotenone induction than taurine treatment alone and action may be mediated via anti-oxidative mechanisms [86]. In a rotenone-induced rat model, taurine significantly ameliorated rotenone-induced decreases in the levels of catecholamine neurotransmitters and tyrosine hydroxylase. It also attenuated rotenone-induced catalase and lipid peroxidation levels [87]. In PC12?cells, treatment with taurine produced protection against toxic agent-induced degeneration [[88], [89], [90]]. Taurine also restored reduced Bcl-2 expression in an H2O2-induced model. It reduced H2O2-induced upregulation of binding immunoglobulin protein (GRP78), growth arrest and DNA damage 153 (GADD153)/C/EBP homologous protein (CHOP) and Bim, signifying that taurine may also play a preventive role against oxidative stress by decreasing ER stress [88]. Against perfluorooctane sulfonate-induced degeneration, administration of taurine also displayed protective activity in PC12?cells. Taurine reduced reactive oxygen species (ROS) production and attenuated perfluorooctane sulfonate-induced increases in autophagy and apoptosis [89]. Moreover, treatment significantly reversed the decrease in viability, oxidative stress and abnormal autophagy in PC12?cells exposed to BDE 209 [90]. Taurine also exhibited protective activity against MPP+-induced neurodegeneration in coronal slices from rat brains. Concentrations of taurine at 1 and 20?mM displayed a potentially protective role in cases of neuronal insult [91]. A recent study described taurine's potential effects against neurodegeneration in a PD model. Taurine protects manganese-induced neuronal injury during the physiological outcome of a cilio-inhibitory dopaminergic system in Crassostrea virginica [92]. In a paraquat- and maneb-induced neurotoxicity model of mice, treatment with taurine (150?mg/kg, i.p.) attenuated a paraquat- and maneb-mediated decrease in tyrosine hydroxylase-positive neurons in the locus coeruleus. Taurine ameliorated toxin-induced microglial activation and M1 polarization as well as proinflammatory cytokine release in the brainstem of mice. Treatment with taurine also prevented the activation of microglial NADPH oxidase and oxidative damage in paraquat- and maneb-intoxicated mice. In addition, inhibiting NF-?B, but not signal transducers, and activators of the transcription 1/3 (STAT1/3) signaling pathway contributed to taurine-prevented microglial activation [93].

Apart from AD and PD models, taurine treatment produced neuroprotective activity against 3-nitropropionic acid (3-NP)-mediated neuronal cell death in a Huntington's disease model [94,95]. Pretreatment (200?mg/kg, 3 days) with taurine ameliorated behavioral dysfunctions and increased GABA concentration in comparison with 3-NP-induced animals. Treatment also displayed activity against 3-NP-induced oxidative stress as shown by decreased striatal malondialdehyde and increased striatal GSH levels. Moreover, it significantly increased the activity of succinate dehydrogenase compared to that in 3-NP-administered animals. Taken together, taurine neuroprotection in a current Huntington's disease model is due, at least partially, to its indirect antioxidant activity and GABA agonistic action [94]. In another study, taurine exhibited less glial fibrillary acidic protein, SOD, and taurine immunoreactivity, together with increased survival rates in 3-NP-induced rats [95]. In an amyotrophic lateral sclerosis model, it protected cultured motor neurons from glutamate-induced neurotoxic injury [96]. Taurine protected motor neuron loss in amyotrophic lateral sclerosis transgenic mice, in which heat shock factor 1-mediated T

[ofonorow]

TAURINE FOR PARKINSON'S DISEASE

After learning that "Chem Trails" are the deliberate release of toxic chemical wastes into the atmosphere, we started developing a new Detox product to be called DETOX-C (tm). The requirement for an ingredient Sulphur, i.e. sulfur containing aminos, such as cysteine and methionine) comes from reading TOXIC LEGACY by Senoff, a book about the problem with pesticides containing glyphosates.

This led to the normally non-essential amino Taurine (which the body makes from cysteine and methionine ) . This research led to the finding of Taurines benefit for Parkinson's:

Taurine and its analogs in neurological disorders: Focus on therapeutic potential and molecular mechanisms

https://www.sciencedirect.com/science/article/pii/S2213231719301971#:~:text=Taurine%20is%20a%20sulfur-containing%20amino%20acid%20and%20known,and%20demonstrates%20extensive%20physiological%20activities%20within%20the%20body.

4. Therapeutic potential of taurine against neurological disorders


4.2. Role in neurodegenerative diseases

.
.
.

In addition to the AD model, the neuroprotective action of taurine against Parkinson's disease (PD) has been studied in cellular and animal models. Taurine exerted an ameliorating action against rotenone-induced neurodegeneration [86,87]. It displayed a concentration-dependent reduction in rotenone-induced cell damage in SH-SY5Y cells. The combination of a subeffective dose of taurine and low and subeffective doses of N-acetyl cysteine afforded better cytoprotection against rotenone induction than taurine treatment alone and action may be mediated via anti-oxidative mechanisms [86]. In a rotenone-induced rat model, taurine significantly ameliorated rotenone-induced decreases in the levels of catecholamine neurotransmitters and tyrosine hydroxylase. It also attenuated rotenone-induced catalase and lipid peroxidation levels [87]. In PC12?cells, treatment with taurine produced protection against toxic agent-induced degeneration [[88], [89], [90]]. Taurine also restored reduced Bcl-2 expression in an H2O2-induced model. It reduced H2O2-induced upregulation of binding immunoglobulin protein (GRP78), growth arrest and DNA damage 153 (GADD153)/C/EBP homologous protein (CHOP) and Bim, signifying that taurine may also play a preventive role against oxidative stress by decreasing ER stress [88]. Against perfluorooctane sulfonate-induced degeneration, administration of taurine also displayed protective activity in PC12?cells. Taurine reduced reactive oxygen species (ROS) production and attenuated perfluorooctane sulfonate-induced increases in autophagy and apoptosis [89]. Moreover, treatment significantly reversed the decrease in viability, oxidative stress and abnormal autophagy in PC12?cells exposed to BDE 209 [90]. Taurine also exhibited protective activity against MPP+-induced neurodegeneration in coronal slices from rat brains. Concentrations of taurine at 1 and 20?mM displayed a potentially protective role in cases of neuronal insult [91]. A recent study described taurine's potential effects against neurodegeneration in a PD model. Taurine protects manganese-induced neuronal injury during the physiological outcome of a cilio-inhibitory dopaminergic system in Crassostrea virginica [92]. In a paraquat- and maneb-induced neurotoxicity model of mice, treatment with taurine (150?mg/kg, i.p.) attenuated a paraquat- and maneb-mediated decrease in tyrosine hydroxylase-positive neurons in the locus coeruleus. Taurine ameliorated toxin-induced microglial activation and M1 polarization as well as proinflammatory cytokine release in the brainstem of mice. Treatment with taurine also prevented the activation of microglial NADPH oxidase and oxidative damage in paraquat- and maneb-intoxicated mice. In addition, inhibiting NF-?B, but not signal transducers, and activators of the transcription 1/3 (STAT1/3) signaling pathway contributed to taurine-prevented microglial activation [93].

Apart from AD and PD models, taurine treatment produced neuroprotective activity against 3-nitropropionic acid (3-NP)-mediated neuronal cell death in a Huntington's disease model [94,95]. Pretreatment (200?mg/kg, 3 days) with taurine ameliorated behavioral dysfunctions and increased GABA concentration in comparison with 3-NP-induced animals. Treatment also displayed activity against 3-NP-induced oxidative stress as shown by decreased striatal malondialdehyde and increased striatal GSH levels. Moreover, it significantly increased the activity of succinate dehydrogenase compared to that in 3-NP-administered animals. Taken together, taurine neuroprotection in a current Huntington's disease model is due, at least partially, to its indirect antioxidant activity and GABA agonistic action [94]. In another study, taurine exhibited less glial fibrillary acidic protein, SOD, and taurine immunoreactivity, together with increased survival rates in 3-NP-induced rats [95]. In an amyotrophic lateral sclerosis model, it protected cultured motor neurons from glutamate-induced neurotoxic injury [96]. Taurine protected motor neuron loss in amyotrophic lateral sclerosis transgenic mice, in which heat shock factor 1-mediated T

[ofonorow]

Medical Medium on Parkinson's
https://www.medicalmedium.com/blog/true-cause-of-parkinsons

[ofonorow]

[ofonorow]

[ofonorow]

[ofonorow]

Either I am losing it (probable) or edoc has removed some of his very interesting posts. Sigh.

There is great value in knowing the root cause of Parkinson's: Combinations of heavy metal toxins in the brain.

According to the ancient source, the brain operates as an electricity grid, and sounds much like today's technology. It runs on electricity, has to be cooled, and perhaps most importantly, while it requires trace minerals and electrolytes and certain hormones to operate, anything that disrupts the flow of electricity disrupts thought and normal brain activity. The toxic heavy metals, such as mercury, aluminum, copper, etc. interfere with the flow of electricity.

[eDOC]

[eDOC]

It's as important in neurodegenerative disorders as in cardiovascular.

IF a person aged approx. +50, has high levels i.e. persistently +150, to achieve a cure, LTP modalities are different vs. those with a normal Calcium score i.e. below 20.

Additionally is easier to cure, provide LTP in the normal groups vs. those in high groups.

Modalities differ for both, and are more time consuming for the raised group ones.

Was going through my records of patients treated, without employing stem cell.

eDOC!!

[ofonorow]

[ofonorow]

[eDOC]

I hope that the high dose B1 works for you. If not I have a 3 month cure protocol, which isn't expensive (Btw- which I would gift), the issue is sending (Customs won't allow it to go through). Since you know am not in Fl, atm, 2 options, either I bring it along or send through a friend, if B1 or your other modalities fail in providing a cure.


eDOC!!

[ofonorow]

I am publicly announcing that I have invented a cure for Parkinson's disease for purpose of establishing the date of Friday, 13 2023 and the matter of prior art when we do the patent. (Really yes, I invented it yesterday, but Friday the 13th is too good to pass up.)

I have to do a patent search , and come to think of it a Google search to see whether someone is already selling the product.

Should we file/receive a patent, it would be like Paulings Lp(a) patents, so somebody can't come along later and claim they invented it. Pharma would never be that unethical, so I'm sure there is nothing to worry about. It would also ensure that someone couldn't use their same patent to block us from selling what will be a new product. Etc.

BTW it won't strictly be a cure, all symptoms will be relieved, so long as the product is continued. Much like Pauling's "cure" for heart disease. Stop vitamin C and lysine at the correct dosage, and the disease process and symptoms return.

Thanks Edoc for the previous post, while my wife is diagnosed, she has few of the expected symptoms, e.g., she doesn't have tremors, she is calm and never gets angry, depressed, fatigued. She has the rigidness on one side, arm and leg, that was the reason for the diagnosis.

Her other mental issues, no short term memory and barely discernable cognitive function, probably won't be remediated by the invention. Will see and that would be more than pleasant if I'm wrong.

I should provide the high level idea I suppose. There exists a treatment that works in all tested via injection. Orally may work, but due to the the theory of the disease etiology, the oral results are hit and miss. The invention guarantees the effectiveness of oral administration.

So it turns out the inventor of high dose Vitamin C therapy, Frederick Klenner, MD, also had important protocols in the 1940s featuring vitamin B1.

And people may forget that Paul Merricks protocol to treat sepsis includes vitamin B1 (thiamine). Who knows, B1 may be the secret weapon.

And former super-contributer Jonwen always seemed to include B1. I didn't know much about B1 until I read a book by anti-aging expert [lookup name and author] who did not believe telomers were that important for staying young and for life extension. A side issue. Actually the book wound up proving to me they are the key, by default by going over everything else known to keep cells younger. He even admitted it himself...maybe it is telomeres .. Had q thorough and rigorous section on vitamin B1. I remember being blown away by what it does, what is known, and what I didn't kniow.